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Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling

Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling

Published on: October 14, 2021

Imbalanced IL-1B and IL-18 Expression in Sézary Syndrome.

Kelly Cristina Gomes Manfrere¹, Marina Passos Torrealba¹, Frederico Moraes Ferreira²

¹Laboratory of Medical Investigation LIM 56, Tropical Medicine Institute of São Paulo, University of São Paulo Medical School, São Paulo 05403-000, Brazil.

International Journal of Molecular Sciences

|March 11, 2023

Summary

Sézary syndrome (SS) involves abnormal skin inflammation. This study reveals an imbalance of IL-1B and IL-18 cytokines in SS patients, suggesting altered inflammasome activation in cutaneous T-cell lymphoma.

Keywords:

IL-18 IL-1B Sézary syndrome erythroderma skin inflammasome lymph nodes

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Area of Science:

Immunology
Dermatology
Oncology

Background:

Sézary syndrome (SS) is an aggressive cutaneous T-cell lymphoma characterized by skin inflammation.
Interleukin-1 beta (IL-1B) and Interleukin-18 (IL-18) are key immune signaling cytokines regulated by inflammasomes.
Dysregulation of these cytokines may contribute to the pathogenesis of SS.

Purpose of the Study:

To investigate the protein and transcript expression of IL-1B and IL-18 in SS patients.
To assess these cytokines as potential markers of inflammasome activation in SS.
To explore the compartmentalized expression patterns of IL-1B and IL-18 in SS.

Main Methods:

Analysis of skin, serum, peripheral mononuclear blood cells (PBMCs), and lymph node samples from SS patients and controls (healthy donors and idiopathic erythroderma).
Assessment of IL-1B and IL-18 protein and transcript levels.
Transcriptomic and pathway analysis of lymph node samples.

Main Results:

Differential protein expression of IL-1B and IL-18 was observed across skin layers (epidermis vs. dermis) in SS patients.
Advanced stage SS lymph nodes showed increased IL-18 and decreased IL-1B protein levels.
Transcriptomic analysis revealed decreased expression of IL1B and NLRP3, with further downregulation of IL1B-associated genes in SS and IE nodes.

Conclusions:

The study provides the first evidence of compartmentalized and imbalanced IL-1B and IL-18 expression in Sézary syndrome.
These findings highlight the potential role of inflammasome dysregulation in SS pathogenesis.
Altered IL-1B and IL-18 expression may serve as potential biomarkers for SS.